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CPT > L11 - NSAIDs > Flashcards

L11 - NSAIDs Flashcards

1
Q

Eicosanoids

A

Prostanoids

Lipoxygenase

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2
Q

Prostanoids

A

Produced locally on demand with a short half life for fine control

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3
Q

PGE2

A

Secreted for gastrointestinal mucosal protection

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4
Q

PGI2 - prostacyclin

A

Inhibits platelet aggregation

Vasodilator

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5
Q

TXA2 - thromboxane A2

A

Platelet aggregation

Vasoconstrictor

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6
Q

Arachidonic acid

A

Derived primarily from dietary linoleic acid in vegetable oils and supplements

  • converted hepatically into arachidonic acid and incorporated into phospholipids
  • found through out the body - muscle, brain and liver
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7
Q

COX -1 homeostatic function

A
  • active across most tissues
  • platelets only contain COX 1 therefore platelet aggregation via TXA2
  • gastrointestinal mucosal protection - PGE2
  • vascular resistance - vasoconstriction- TXA2
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8
Q

COX 1 pathological function

A

Chronic inflammation
Chronic pain
Raised blood pressure - vasoconstriction THXA2

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9
Q

COX 2 homeostatic function

A

Inducibke mostly in the brain, kidney and bone

Renal homeostasis
Tissue repair and healing
Reproduction - uterine contractions
Inhibition of platelet aggregation - PGI2 (prostacyclin)

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10
Q

COX 2 pathological functions

A 
Chronic inflammation 
Chronic pain 
Fever 
Blood vessel permeability 
Tumour cell growth
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11
Q

How do prostanoids exert their effects?

A

Action is local at GPCRs

Specific action dependent on receptor subtype and location

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12
Q

Imbalance between TXA2 and PGI2

A 
TXA2 and PGI2 antagonise each other 
Imbalance can cause:
- hypertension 
- MI 
- Stroke
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13
Q

Diet rich in fish oils (omega FAs)

A

Omega fatty acids are converted to TXA3 and PGI3

Better prostanoids with lower incidence of CVD

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14
Q

Effects of NSAIDs

A

Analgesic
Anti- inflammatory
Anti - pyretic

By inhibiting prostaglandins

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15
Q

NSAID mechanism of action

A

Inhibition of COX - competes with arachidonic acid for the hydrophobic site of COX
Decrease in prostanoids - prostaglandin, prostacyclin and thromboxane synthesis

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16
Q

Analgesic property

A
  • Local peripheral action at site of pain
  • works better when inflamed as more prostaglandins present
  • blocks PGE2 therefore reduces peripheral pain fibre sensitivity
  • less PGE2 synthesis in dorsal horn so less neurotransmitter released
    Therefore less excitability of neurones in the pain pathways
  • full efficacy after several days of dosing
17
Q

Anti inflammatory effect

A

NSAIDs reduced the production of prostaglandins released during injury therefore less vasodilation and oedema

  • decreases local swelling and permeability
  • relieves symptoms but not the cause
18
Q

Antipyretic properties

A

Inhibition of hypothalamic COX 2

Therefore less cytokine (IL1 and IL6) induced prostaglandin synthesis, reducing temperature

19
Q

PGE2 and temperature

A

PGE2 contributes to the thermoregulatory centre, increasing set point and raising the temperature in the preoptic area of the hypothalamus

Stimulated by pyrogens - IL1 and IL6

20
Q

COX2 inhibitor selectivity

A

Are more selective than COX 1 at therapeutic dose

21
Q

NSAIDs

A

Aspirin
Ibuprofen
Naproxen
Diclofenac

COX 2 selective: bigger structure binds to the COX2 binding pocket

  • celecoxib
  • etoricoxib
22
Q

Gastrointestinal ADRs

A
  • dyspepsia
  • nausea
  • peptic ulceration
  • bleeding and perforation
  • exacerbation of IBD
  • local irritation and bleeding from rectal administration

Due to:
- decreased mucosal and bicarbonate secretion
- decreased mucosal blood flow - enhanced cytotoxicity and hypoxia
- increased acid secretion
-

23
Q

Cautions with NSAIDs

A
  • Elderly - often self prescribing or meds not reviewed
  • prolonged use
  • Glucocorticoid steroids - given PPI as adjunct
  • anticoagulants
  • smoking
  • alcohol
  • history of peptic ulceration
  • H. pylori
24
Q

Renal ADRs

A
  • NSAIDs inhibit prostaglandin
  • Prostaglandin normally causes vasodilation of the afferent arterioles to increase GFR and inhibit sodium absorption in the collecting duct
  • As inhibited, GFR decreases and renal blood flow decreases
  • increased sodium and water absorption - increasing BP

Caution in patients with CKD and heart failure as low BP, therefore greater reliance on prostaglandins for vasodilation and renal perfusion

25
Q

Considerations

A

antihypertensives:

  • ace inhibitor - dilates the efferent arterioles and constricts the afferent arteriole which will decrease GFR
  • ARBs
  • diuretics

Class II effect

  • sulfonylureas
  • warfarin
  • methotrexate
  • CVD risk
  • renal function and age
  • level of pain, inflammation and Pyrex is
  • GI disease
26
Q

COX 2 inhibitor mechanism of action

A

Just inhibits COX2 mediated PGI2 synthesis

  • unopposed TXA2 - prothrombotic therefore increases CVD risk
  • Avoids COX1 homeostatic actions therefore less GI ADRs as PGE2 not affected
27
Q

When are COX 2 used

A

Osteoarthritis

Rheumatoid arthritis

28
Q

NSAIDs and protein binding

A 
Highly protein bound therefore class II effect 
Displaces other bound drugs, increasing free drug concentration of:
  • sulfonylurea - can cause hypoglycaemia
  • methotrexate - can cause accumulation and hepatotoxicity, leukopenia and rheumatoid arthritis
  • warfarin - increases risk of ble3dinf
29
Q

Uses of NSAIDs

A 
Inflammatory conditions 
Osteoarthritis - topical NSAID 
Postoperative pain 
Topical use on cornea 
Menorrhagia
30
Q

Paracetamol

A
  • antipyretic
  • mild to moderate analgesic

COX2 selective inhibition in spinal cord (CNS) - decreased pain signal to higher centres

Per oxidases in peripheral inflammation inhibit paracetamol therefore not anti inflammatory

31
Q

Half life of paracetamol

A

2 hours

Activated by conjugation in the liver

32
Q

Paracetamol overdose

A

Normally conjugated with glutathione but exceeds hepatic capacity

Build up of NAPQI - highly nucleophilic which oxidises key metabolic enzymes causing cell death

33
Q

Dose that causes damage

A

150mg/kg

34
Q

Treatment of paracetamol overdose

A

N- acetylcysteine- after 4 hours of dose

- donates glutathione to increase phase 2 metabolism of paracetamol
Glutathione is not absorbed by hepatocytes

35
Q

Presentation of paracetamol overdose

A

24 hours:
Nausea
Vomiting
Abdominal pain

Maximal liver damage - 3 to 4 days

CPT (23 decks)

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